DNAI converts multi-omics and pathology data into physics-constrained digital twins — enabling oncologists and biopharma to compare treatment scenarios with quantified uncertainty.
Compare therapy options for your patient. See simulated trajectories with confidence intervals and rationale.
Explore clinical toolsForecast trial outcomes, generate virtual control arms, and stratify cohorts — before enrollment begins.
Explore trial toolsStratify cohorts, discover biomarkers, and validate hypotheses. Interpretable simulations with structured abstention.
Explore research toolsEvaluated across multiple independent cohorts. Every simulation is constrained by biological law — performance reported per cancer type and modality.
Tumor growth rates, drug sensitivity, and immune parameters are bounded to biologically plausible ranges. Outputs that violate physical constraints are rejected.
Every simulation traces to specific genes, pathways, and physics parameters. Driver gene rankings, pathway-level attributions, and uncertainty intervals — not a black-box score.
21 CFR Part 11 audit trail, calibrated probabilities, and signed execution tokens. Designed for regulatory compatibility.
When patient data is insufficient or out-of-distribution, the system flags uncertainty and explains what is missing — rather than forcing a prediction.
Three steps from patient data to actionable simulation.
RNA-seq, DNA mutations, CNV, methylation, histopathology — the platform ingests what you already have. Probabilistic fusion handles missing modalities; best results with matched pathology (WSI).
A patient-specific tumor model simulates growth, drug response, resistance timing, and immune dynamics — all constrained by biological physics.
Ranked treatment options with survival projections, confidence intervals, and the specific genes and pathways driving each simulation.
Unlike black-box AI, DNAI simulations are constrained by biological physics.
Growth rates, drug sensitivity, and immune parameters are bounded to biologically plausible ranges. If data is insufficient, the system abstains and explains what is missing — rather than guessing.
Most oncology AI predicts static risk. DNAI simulates treatment scenarios, quantifies reliability, and abstains when evidence is insufficient — backed by mechanistic constraints and external validation.
Reliability-gated, counterfactual digital twins that simulate tumor dynamics per patient
Don't just predict risk — simulate the remedy. We model 6 distinct treatment scenarios for every patient to rank options by potential benefit under uncertainty.
Engineered to abstain when data is insufficient. Every patient receives a High / Medium / Low reliability score based on information sufficiency — not a forced prediction.
Not just pattern-matching — tumor dynamics. We use differential equations with bounded biological parameters: proliferation, drug sensitivity, and immune killing. Predictions are plausible by design.
Tested where it matters — outside the training data. Multi-site external cohorts with per-patient reliability checks, not just internal cross-validation. Performance varies by cancer type and modality.
Our patented Domain Separation Network bridges preclinical mouse models to human biology — removing species-specific stroma while preserving tumor signal. Translate PDX efficacy signals toward human endpoints for research prioritization.
Research use only. Not cleared or approved for clinical decision-making. Survival estimates based on observational counterfactual modeling.
Simulation-informed treatment planning
Visualize likely outcomes for Standard of Care vs. experimental agents before making treatment decisions.
"Alert: Subpopulation 3 projected to drive resistance to Therapy A by Day 180." Plan adaptive strategies proactively.
Explore dosing schedules that balance efficacy and safety constraints — optimized through the differentiable tumor model.
In silico trials and mechanism discovery
Generate physics-constrained synthetic patient trajectories for control arms. Modeled potential to reduce control-arm enrollment by 30–50% — enabling more patients to receive experimental treatments.
Use the Driver module to understand why a drug works in Subgroup A but fails in Subgroup B. Identify predictive biomarkers.
Identify the specific dosing schedule or patient subpopulation required to make a failed compound effective.
From patient dashboard to tumor evolution simulations — explore the DNAI interface.
See how DNAI can transform your oncology workflows.